Helsinki, Finland
Helsinki, Finland

The University of Helsinki is a university located in Helsinki, Finland since 1829, but was founded in the city of Turku in 1640 as the Royal Academy of Turku, at that time part of the Swedish Empire. It is the oldest and largest university in Finland with the widest range of disciplines available. Around 36,500 students are currently enrolled in the degree programs of the university spread across 11 faculties and 11 research institutes.As of August 1, 2005, the University complies with the standards of the Europe-wide Bologna Process and offers Bachelor, Master, Licenciate, and Doctoral degrees. Admission to degree programmes is usually determined by entrance examinations, in the case of bachelor degrees, and by prior degree results, in the case of master and postgraduate degrees. Entrance is particularly selective . It has been ranked a top 100 university in the world according to the 2012 QS, Times Higher Education and the Academic Rankings of World Universities.The university is bilingual, with teaching provided both in Finnish and Swedish. Teaching in English is extensive throughout the university at Master, Licentiate, and Doctoral levels, making it a de facto third language of instruction.Remaining true to its traditionally strong Humboldtian ethos, the University of Helsinki places heavy emphasis on high-quality teaching and research of a top international standard. It is a member of various prominent international university networks, such as Europaeum, UNICA, the Utrecht Network, and is a founding member of the League of European Research Universities. Wikipedia.


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Patent
University of Helsinki | Date: 2015-05-18

The present invention relates to adenoviral vectors, wherein the viral capsid has been coated with polypeptides, which are capable of stimulating a peptide-specific immune response in a subject and uses thereof. Furthermore, the present invention relates to methods of treating diseases, e.g. cancer, by adenoviral vectors which have been coated by polypeptides causing peptide-specific immune response. Also the present invention relates to a method of coating adenoviral vectors by specific peptides as well as to a method of identifying those peptides suitable for coating the capsid of an adenoviral vector.


This invention relates to bioassay method wherein the presence of a specific soluble antibody in a sample of a bodily fluid, preferably plasma or serum, of an animal, including human, is qualitatively and/or quantitatively determined. The method employs, a first group labelled with an energy donor and a second group labelled with an energy acceptor; the first group, or second group, comprising an antigen of the soluble antibody and the second group, or first group, respectively, comprising a Fab binding moiety capable of binding to a Fab region of antibodies of said animal. The donor and the acceptor form an energy transfer pair capable of energy transfer. The invention further comprises a kit for the bioassay method.


Nunnari J.,University of California at Davis | Suomalainen A.,University of Helsinki
Cell | Year: 2012

Mitochondria perform diverse yet interconnected functions, producing ATP and many biosynthetic intermediates while also contributing to cellular stress responses such as autophagy and apoptosis. Mitochondria form a dynamic, interconnected network that is intimately integrated with other cellular compartments. In addition, mitochondrial functions extend beyond the boundaries of the cell and influence an organism's physiology by regulating communication between cells and tissues. It is therefore not surprising that mitochondrial dysfunction has emerged as a key factor in a myriad of diseases, including neurodegenerative and metabolic disorders. We provide a current view of how mitochondrial functions impinge on health and disease. © 2012 Elsevier Inc.


Grant
Agency: European Commission | Branch: H2020 | Program: RIA | Phase: INFRAIA-01-2016-2017 | Award Amount: 10.00M | Year: 2017

Experimentation in mesocosms is arguably the single most powerful approach to obtain a mechanistic quantitative understanding of ecosystem-level impacts of stressors in complex systems, especially when embedded in long-term observations, theoretical models and experiments conducted at other scales. AQUACOSM builds on an established European network of mesocosm research infrastructures (RI), the FP7 Infra project MESOAQUA (2009-2012), where 167 users successfully conducted 74 projects. AQUACOSM greatly enhances that network on pelagic marine systems in at least 3 ways: first by expanding it to 10 freshwater (rivers and lakes), 2 brackish and 2 benthic marine facilities, and by involving 2 SMEs and reaching out to more, thereby granting effective transnational access to world-leading mesocosm facilities to >340 users on >11500 days; second, by integrating scattered know-how between freshwater and marine RI; and third, by uniting aquatic mesocosm science in an open network beyond the core consortium, with industry involved in an ambitious innovation process, to promote ground-breaking developments in mesocosm technology, instrumentation and data processing. A new dimension of experimental ecosystem science will be reached by coordinated mesocosm experiments along transects from the Mediterranean to the Arctic and beyond salinity boundaries. These efforts will culminate in a joint research activity (JRA) to assess aquatic ecosystem responses across multiple environmental gradients to a selected climate-related key stressor with repercussions for ecosystem services. Overall, AQUACOSM will fill a global void by forging an integrated freshwater and marine research infrastructure network. Long-term sustainability is sought through assessing governance models based on science priorities and economic innovation opportunities. Linkages to and synergies with ESFRI RI and other large initiatives are ensured by AQUACOSM partners and Advisory Board members in those programs.


Grant
Agency: European Commission | Branch: H2020 | Program: RIA | Phase: SC1-PM-01-2016 | Award Amount: 15.04M | Year: 2017

The complex interactions between genetic and non-genetic factors produce heterogeneities in patients as reflected in the diversity of pathophysiology, clinical manifestations, response to therapies, disease development and progression. Yet, the full potential of personalized medicine entails biomarker-guided delivery of efficient therapies in stratified patient populations. MultipleMS will therefore develop, validate, and exploit methods for patient stratification in Multiple Sclerosis, a chronic inflammatory disease and a leading causes of non-traumatic disability in young adults, with an estimated cost of 37 000 per patient per year over a duration of 30 years. Here we benefit from several large clinical cohorts with multiple data types, including genetic and lifestyle information. This in combination with publically available multi-omics maps enables us to identify biomarkers of the clinical course and the response to existing therapies in a real-world setting, and to gain in-depth knowledge of distinct pathogenic pathways setting the stage for development of new interventions. To create strategic global synergies, MultipleMS includes 21 partners and covers not only the necessary clinical, biological, and computational expertise, but also includes six industry partners ensuring dissemination and exploitation of the methods and clinical decision support system. Moreover, the pharmaceutical industry partners provide expertise to ensure optimal selection and validation of clinically relevant biomarkers and new targets. Our conceptual personalized approach can readily be adapted to other immune-mediated diseases with a complex gene-lifestyle background and broad clinical spectrum with heterogeneity in treatment response. MultipleMS therefore goes significantly beyond current state-of-the-art thereby broadly affecting European policies, healthcare systems, innovation in translating big data and basic research into evidence-based personalized clinical applications.


Meretoja A.,University of Helsinki
Neurology | Year: 2012

Efficacy of thrombolytic therapy for ischemic stroke decreases with time elapsed from symptom onset. We analyzed the effect of interventions aimed to reduce treatment delays in our single-center observational series. All consecutive ischemic stroke patients treated with IV alteplase (tissue plasminogen activator [tPA]) were prospectively registered in the Helsinki Stroke Thrombolysis Registry. A series of interventions to reduce treatment delays were implemented over the years 1998 to 2011. In-hospital delays were analyzed as annual median door-to-needle time (DNT) in minutes, with interquartile range. A total of 1,860 patients were treated between June 1995 and June 2011, which included 174 patients with basilar artery occlusion (BAO) treated mostly beyond 4.5 hours from symptom onset. In the non-BAO patients, the DNT was reduced annually, from median 105 minutes (65-120) in 1998, to 60 minutes (48-80) in 2003, further on to 20 minutes (14-32) in 2011. In 2011, we treated with tPA 31% of ischemic stroke patients admitted to our hospital. Of these, 94% were treated within 60 minutes from arrival. Performing angiography or perfusion imaging doubled the in-hospital delays. Patients with in-hospital stroke or arriving very soon from symptom onset had longer delays because there was no time to prepare for their arrival. With multiple concurrent strategies it is possible to cut the median in-hospital delay to 20 minutes. The key is to do as little as possible after the patient has arrived at the emergency room and as much as possible before that, while the patient is being transported.


Pyykko P.,University of Helsinki
Chemical Reviews | Year: 2012

Quantum electrodynamics (QED) is the orders of magnitude below the Dirac-level relativistic effects and, being small, thus indirectly verifies the soundness of the latter. For neutral or nearly neutral systems, beyond Li, only one order-of-magnitude improvement of the computational accuracy, mainly the treatment of electron correlation with adequate basis sets, is estimated to separate the QED effects from being observed in head-on comparisons of theory and experiment. If the zero-point oscillations of the EM field are modified by objects ranging from molecules to macroscopic bodies, this leads to Casimir forces between them. The width of the chosen self-energy (SE) potential is arbitrary and could range from nuclear dimensions to much more diffuse values. Reviews on the finite nuclear charge distributions and their inclusion in quantum chemistry show that an explicit, quantum-mechanical description of both the nucleus and the electrons, is required.


Alitalo K.,University of Helsinki
Nature Medicine | Year: 2011

Blood vessels form a closed circulatory system, whereas lymphatic vessels form a one-way conduit for tissue fluid and leukocytes. In most vertebrates, the main function of lymphatic vessels is to collect excess protein-rich fluid that has extravasated from blood vessels and transport it back into the blood circulation. Lymphatic vessels have an important immune surveillance function, as they import various antigens and activated antigen-presenting cells into the lymph nodes and export immune effector cells and humoral response factors into the blood circulation. Defects in lymphatic function can lead to lymph accumulation in tissues, dampened immune responses, connective tissue and fat accumulation, and tissue swelling known as lymphedema. This review highlights the most recent developments in lymphatic biology and how the lymphatic system contributes to the pathogenesis of various diseases involving immune and inflammatory responses and its role in disseminating tumor cells. © 2011 Nature America, Inc. All rights reserved.


Pyykko P.,University of Helsinki
Annual Review of Physical Chemistry | Year: 2012

Relativistic effects can strongly influence the chemical and physical properties of heavy elements and their compounds. This influence has been noted in inorganic chemistry textbooks for a couple of decades. This review provides both traditional and new examples of these effects, including the special properties of gold, lead-acid and mercury batteries, the shapes of gold and thallium clusters, heavy-atom shifts in NMR, topological insulators, and certain specific heats. © Copyright ©2012 by Annual Reviews. All rights reserved.


Rajala H.L.,University of Helsinki
Blood | Year: 2013

Large granular lymphocytic (LGL) leukemia is characterized by clonal expansion of cytotoxic T cells or natural killer cells. Recently, somatic mutations in the signal transducer and activator of transcription 3 (STAT3) gene were discovered in 28% to 40% of LGL leukemia patients. By exome and transcriptome sequencing of 2 STAT3 mutation-negative LGL leukemia patients, we identified a recurrent, somatic missense mutation (Y665F) in the Src-like homology 2 domain of the STAT5b gene. Targeted amplicon sequencing of 211 LGL leukemia patients revealed 2 additional patients with STAT5b mutations (N642H), resulting in a total frequency of 2% (4 of 211) of STAT5b mutations across all patients. The Y665F and N642H mutant constructs increased the transcriptional activity of STAT5 and tyrosine (Y694) phosphorylation, which was also observed in patient samples. The clinical course of the disease in patients with the N642H mutation was aggressive and fatal, clearly different from typical LGL leukemia with a relatively favorable outcome. This is the first time somatic STAT5 mutations are discovered in human cancer and further emphasizes the role of STAT family genes in the pathogenesis of LGL leukemia.

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